+ Models PNEC-1879; No. of Pages 8 Please cite this article in press as: McFarlane, A.C., et al., Cortisol response to acute trauma and risk of posttraumatic stress disorder. Psychoneuroendocrinology (2010), doi:10.1016/j.psyneuen.2010.10.007 Cortisol response to acute trauma and risk of posttraumatic stress disorder Alexander C. McFarlane a , Christopher A. Barton a, * , Rachel Yehuda b , Gary Wittert c a Centre for Military and Veterans Health, School of Population Health and Clinical Practice, The University of Adelaide, South Australia, Australia b Discipline of Medicine, School of Medicine, The University of Adelaide, South Australia, Australia c Mt Sinai School of Medicine, New York, NY, United States Received 23 December 2009; received in revised form 6 October 2010; accepted 12 October 2010 1. Introduction An increasing body of evidence suggests that mounting an adequate cortisol response at the time of exposure to a traumatic event has a protective effect against posttrau- matic stress symptoms (Yehuda, 2002). Yet, practically Psychoneuroendocrinology (2010) xxx, xxx—xxx * Corresponding author at: 2/122 Frome St., Centre for Military and Veterans Health, School of Population Health and Clinical Practice, University of Adelaide, Adelaide, South Australia 5005, Australia. E-mail address: Christopher.barton@adelaide.edu.au (C.A. Barton). KEYWORDS Posttraumatic stress disorder; Cortisol; Dexamethasone; Motor vehicle accident; Depression; Prospective study Summary This study sought to characterize the variability of the acute cortisol response following trauma and its relationship to posttraumatic stress disorder (PTSD). Forty eight participants were recruited within 24 h of a traumatic accident requiring hospital admission. A saliva sample was collected at 08.00 h and 16.00 h 2 days, 1 month and 6 months after hospital admission, together with 24-h urine collection. Participants completed a dexamethasone sup- pression test (0.5 mg DEX at 21.00 h) at each follow up, together with self-report questionnaires. The Clinician Administered PTSD Scale (CAPS) was administered at 1 and 6 months to identify PTSD. Prevalence of PTSD was 27% at 1 month and 21% at 6 months. PTSD symptoms at 6 months were negatively correlated with salivary cortisol at 08.00 h on day 2 (r = 0.36, p = 0.04), but positively correlated with 16.00 h cortisols (r = 0.41, p = 0.03). A lower rise in cortisol at 08.00 h on day 2 was associated with an increase in risk of PTSD at both 1 month (OR = 1.411 (1.017, 1.957)) and 6 months (OR = 1.411 (1.066, 1.866)). At 1 month, 70% of participants with PTSD suppressed cortisol to more than 90% of pre-dex levels compared with 25% without PTSD (x 2 = 6.77, p = 0.034). Urinary cortisol excretion was not different between groups at any time point. The findings support a hypothesis that sensitization of the HPA axis and enhanced suppression of cortisol following the dexamethasone suppression test are established early in the disease process. # 2010 Elsevier Ltd. All rights reserved. available at www.sciencedirect.com journal homepage: www.elsevier.com/locate/psyneuen 0306-4530/$ — see front matter # 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.psyneuen.2010.10.007